Study participants who reported tobacco use or had higher levels of biomarkers of tobacco exposure had a higher prevalence of the sexually transmitted infection, oral human papillomavirus type 16 (HPV-16), according to a study in the October 8 JAMA, a theme issue on infectious disease.
Oral HPV-16 is believed to be responsible for the increase in incidence of oropharyngeal squamous cell cancers in the United States. An association between self-reported number of cigarettes currently smoked per day and oral HPV prevalence has been observed, according to background information in the article.
Carole Fakhry, M.D., M.P.H., of the Johns Hopkins University School of Medicine, Baltimore, and colleagues investigated associations between objective biomarkers reflective of all current tobacco exposures (environmental, smoking, and use of smokeless tobacco) and oral HPV-16 prevalence. The researchers used data from the National Health and Nutrition Examination Survey (NHANES), a probability sample of the U.S. population. Mobile examination center participants ages 14 to 69 years were eligible for oral HPV DNA testing. Computer-assisted self-interviews were used to ascertain self-reported tobacco use and sexual behaviors. Selfreported tobacco use for the past 5 days included any nicotinecontaining product. Biomarkers of recent tobacco use included serum cotinine, a major nicotine metabolite, and urinary 4- (methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), a tobaccospecific, carcinogenic metabolite.
This analysis included 6,887 NHANES participants, of whom 2,012 (28.6 percent) were current tobacco users and 63 (1.0 percent) had oral HPV-16 detected. Current tobacco users were more likely than nonusers to be male, younger, less educated, and to have a higher number of lifetime oral sexual partners. Self-reported and biological measures of tobacco exposure as well as oral sexual behavior were significantly associated with prevalent oral HPV-16 infection. Oral HPV-16 prevalence was greater in current tobacco users (2.0 percent) compared with never or former tobacco users (0.6 percent). Average cotinine and NNAL levels were higher in individuals with vs without oral HPV-16 infection.
"These findings highlight the need to evaluate the role of tobacco in the natural history of oral HPV-16 infection and progression to malignancy," the authors write.